LncRNA prostate androgen-regulated transcript 1 (PART 1) functions as an oncogene in osteosarcoma via sponging miR-20b-5p to upregulate BAMBI

Abstract

Background: Osteosarcoma (OS) is an aggressive bone cancer that most commonly affects adolescents and children. Emerging studies have shown that long noncoding RNA (lncRNA) performs essential roles in the occurrence and development of many tumors. Prostate androgen-regulated transcript 1 (PART 1) has been reported as a tumor oncogene; despite this, the mechanisms underlying its involvement in OS are unclear.Methods: OS and paired normal tissue samples were obtained, and gene expressions were detected by real time-quantitative polymerase chain reaction (RT-qPCR). The functions of PART 1 in OS cell proliferation, invasion, and migration were determined by Cell Counting Kit-8 (CCK-8) and Transwell assays. Furthermore, the binding sites of PART 1 and miR-20b-5p as well as those between miR-20b-5p and bone morphogenic protein and activin membrane-bound inhibitor homolog (BAMBI) were verified by bioinformatics analysis and dual-luciferase reporter assay.Results: Our study found obvious overexpression of PART 1 in OS tissues and cells. Furthermore, PART 1 overexpression facilitated OS cell proliferation, invasion, and migration. Further mechanistic investigations revealed that PART 1 could sponge to miR-20b-5p, which was expressed at a low level in OS tissues and cells. Importantly, miR-20b-5p overexpression inhibited OS cell proliferation, invasion, and migration.Additionally, BAMBI was confirmed as a downstream gene of miR-20b-5p, and its expression was reversely modulated by miR-20b-5p and positively modulated by PART 1. Rescue experiments suggested that BAMBI was involved in PART 1-mediated promotion of OS progression.Conclusions: PART 1 serves as a competing endogenous RNA to promote OS tumorigenesis via its regulation of the miR-20b-5p/BAMBI axis, which may provide a promising therapeutic biomarkers for OS patients.

Regulation of Neuroendocrine-like Differentiation in Prostate Cancer by Non-Coding RNAs

“…  in PCa vs adjacent tissue [244,255]   migration, invasion, EMT [256]   proliferation, migration [255]  poor survival [244]  tissue:  predicts BCR [236]  regulated by lncRNA PART1 [257] hsa-miR-363   in NEPC tissues [194] ---  in recurrent PCa [258]   in young PCa patients [199…”

“…  in PCa vs adjacent tissue [244,255]   migration, invasion, EMT [256]   proliferation, migration [255]  poor survival [244]  tissue:  predicts BCR [236]  regulated by lncRNA PAR [257] hsa-miR-363   in NEPC tissues [194 with an  in malignancy [233]   in PCa vs BPH [263]   in PCa [264] [265]   in PCa and metastases [266]   viability, migration, invasion [264]  overrides radiation-induced cell cycle arrest [267]  associated with disease recurrence [266] --  in PCa [199]   in patients with LN metastases [269]  promotes PCa progression [270,271]   expression predicts poor survival [272]  blood: BPH vs PCa   favors progression and self-renewal [129]   correlates with early clinical failure [286]  urine: cancer cellmacrophage signalling [287]  urine: PCa vs healthy [288]  negative regulation by lncRNA TTTY15 [289]  suppresses AR via Myc [290] in NED in vitro [228] --• PTEN [254] •…”

“…PCa [258]   in young PCa patients [199]   in expression concomitantly   proliferation and EMT [259] predicts BCR [236] • regulated by lncRNA PART1 [257] hsa-miR-363…”

“…  in PCa vs adjacent tissue [244,255]   migration, invasion, EMT [256]   proliferation, migration [255]  poor survival [244]  tissue:  predicts BCR [236]  regulated by lncRNA PART1 [257] hsa-miR-363   in NEPC tissues [194] ---  in recurrent PCa [258]   in young PCa patients [199]   in expression concomitantly   proliferation and EMT [259] -- miR-363 biogenesis regulated by IFIT5, downstream of IFNgammaantiviral response) [189] in malignancy [233] •   in experimental NED [228]  PTEN [230]  RB1 [231] [232]   expression with  malignity [233]   in solid tumours [234] [235]  confers radioresistance [232]  serum: localized PCa vs BPH [237]  serum: low risk vs aggressive PCa [238] HAND2-AS1 [239]  FER1LR [240] hsa-miR-92a --- PTEN…”

“…[249]  TP53 [250]   proliferation [245]  plasma: localized vs metastatic PCa [251]  urine: BCR [252]  urine, urine EVs, plasma: PCa vs BPH vs healthy [246]  biopsy: tumour vs adjacent tissue [253] -- PTEN [254]   in PCa vs adjacent tissue [244,255]   migration, invasion, EMT [256]   proliferation, migration [255]  poor survival [244]  tissue:  predicts BCR [236]  regulated by lncRNA PART1 [257] --  in recurrent PCa [258]   in young PCa patients [199]   in expression concomitantly   proliferation and EMT [259] -- miR-363 biogenesis regulated by IFIT5, downstream of IFNgammaantiviral response) [189] in NED from hypoxia [260] • 12 of 42 with an  in malignancy [233]   in PCa vs BPH [263]   in PCa [264] [265]   in PCa and metastases [266]   viability, migration, invasion [264]  overrides radiation-induced cell cycle arrest [267]  associated with disease recurrence [266] --  in PCa [199]   in patients with LN metastases [269]  promotes PCa progression [270,271]   expression predicts poor survival [272]  blood: BPH vs PCa   favors progression and self-renewal [129]   correlates with early clinical failure [286]  urine: cancer cellmacrophage signalling [287]  urine: PCa vs healthy [288]  negative regulation by lncRNA TTTY15 [289]  suppresses AR via Myc [290] in experimental NED…”